The variability of fetal heart rate is an important clinical indicator of fetal well-being. The study of the regulation of heart rate variability in the compromised fetus has been seriously hampered by the lack of a good animal model. I contend that the fetal sheep behaves similarly to the human fetus during acute hypoxia when the hypoxic influences on myocardial conduction are circumvented. Preliminary data in support of this hypothesis are revealed in the main body of the application. This hypothesis will be further tested by the first project. Six additional hypotheses will be tested to determine what aspects of hypoxia mediate the decrease in fetal heart rate variability during hypoxia. I will test the hypothesis that the autonomic nervous system plays an important role in regulation of heart rate variability. The baroreceptors are another candidate for regulation of heart rate variability. The importance of baroreceptors in the phenomenon will be examined. Cerebral blood flow and metabolite delivery and consumption will be decreased and their effect on heart rate variability determined .The separate effects of decreased oxygen tension, increased carbon dioxide tension and decreased pH will be analyzed for their effects on fetal heart rate variability. I anticipate finding that the balance between the parasympathetic and sympathetic nervous systems and that baroreceptors are important in the later more severe stages of fetal distress. I will also test the hypothesis that increased myocardial adenosine levels play an important role in the regulation of fetal heart rate variability during hypoxia. This theory will be tested by competitive blockade of adenosine receptors. Finally, I will determine the effect of hypoxia on the heart rate variability of fetuses exposed to narcotics.